Acute acquired toxoplasmosis: clinical-laboratorial aspects and ophthalmologic evaluation in a cohort of immunocompetent patients.

Most cases of acute acquired toxoplasmosis (AAT) are oligosymptomatic and self-limited. Therefore, these infections rarely indicate treatment. Prospective studies of AAT patients are rare in the medical literature. The frequency of systemic manifestations has not been sufficiently studied. In order to search for risks factors for systemic and ocular involvement, 37 patients were submitted to a diagnostic investigative protocol. The most frequent findings were lymph node enlargement (94.6%), asthenia (86.5%), headache (70.3%), fever (67.6%) and weight loss (62.2%). Hepatomegaly and/or splenomegaly were present in 21.6% of cases (8/37). Liver transaminases were elevated in 11 patients (29.7%) and lactic dehydrogenase in 17 patients (45.9%). Anaemia was found in four patients (10.8%), leucopoenia in six patients (16.2%), lymphocytosis in 14 patients (37.8%) and thrombocytopenia in one patient (2.7%). Fundoscopic examination revealed retinochoroiditis in four patients (10.8%). No statistical association was found between any one morbidity and retinochoroiditis. Nevertheless, a significant association was found between the presence of more than eight morbidity features at evaluation and long-lasting disease. An ideal diagnostic protocol for AAT would include evidence of systemic involvement. Such a protocol could be used when planning treatment.

Acute acquired toxoplasmosis: clinical-laboratorial aspects and ophthalmologic evaluation in a cohort of immunocompetent patients

Most cases of acute acquired toxoplasmosis (AAT) are oligosymptomatic and self-limited. Therefore, these infections rarely indicate treatment. Prospective studies of AAT patients are rare in the medical literature. The frequency of systemic manifestations has not been sufficiently studied. In order to search for risks factors for systemic and ocular involvement, 37 patients were submitted to a diagnostic investigative protocol. The most frequent findings were lymph node enlargement (94.6 percent), asthenia (86.5 percent), headache (70.3 percent), fever (67.6 percent) and weight loss (62.2 percent). Hepatomegaly and/or splenomegaly were present in 21.6 percent of cases (8/37). Liver transaminases were elevated in 11 patients (29.7 percent) and lactic dehydrogenase in 17 patients (45.9 percent). Anaemia was found in four patients (10.8 percent), leucopoenia in six patients (16.2 percent), lymphocytosis in 14 patients (37.8 percent) and thrombocytopenia in one patient (2.7 percent). Fundoscopic examination revealed retinochoroiditis in four patients (10.8 percent). No statistical association was found between any one morbidity and retinochoroiditis. Nevertheless, a significant association was found between the presence of more than eight morbidity features at evaluation and long-lasting disease. An ideal diagnostic protocol for AAT would include evidence of systemic involvement. Such a protocol could be used when planning treatment.

Progression of acral bone resorption in multibacillary leprosy.

Although leprosy became a curable disease after implementation of the Global Strategy for the Elimination of Leprosy (WHO), mutilations and deformities are still commonplace in endemic countries. Hence, it remains important to evaluate the prevalence rate and the risk factors of acral bone resorption in the multidrug therapy (MDT) era. A cohort of 105 newly-diagnosed adult multibacillary leprosy patients admitted for treatment between 1990-1992 was surveyed until 1999. Progression of bone resorption (BR) in cured leprosy patients was observed up to 8 years after release from MDT. Twenty three percent of the patients were found to have acral resorption. BR was found to be associated with male sex, grade of disability at diagnosis with other deformities and with the occurrence of four or more lepra reactions. Patient surveillance after release from MDT continues to be a necessary procedure in individuals with disabilities and recurrent or persistent reactions.

Neurophysiology of pain-peripheral aspects. Speculation concerning the possibility of a unitary peripheral cutaneous input system for pressure, hot, cold and tissue damage.

The gate theory of pain is criticized at three levels: (1) at the dorsal horn "gate", where pre-synaptic inhibition in the primary afferent endings may go beyond mere reduction of synaptic power at the afferent endings and induce antidromic impulses (dorsal root reflexes) that may modulate peripherally by blocking; (2) central to the "gate", where postsynaptic neuronal repetitive (epileptiform) firing is believed to be an important underlying mechanism in clinical chronic pain syndromes; and, (3) in the periphery, where there is more to input coding than a balance between the ratio of large and smaller fiber inputs. Contrary to the belief of many sensory neurophysiologists, the present authors contend that pattern theory is viable; and that specificity, while important and not to be ignored, should be considered as only a partially evolved refinement superimposed on a basic underlying spatial and temporal patterning of input that probably requires central decoding, which begins in the dorsal horn.

The site of anoxic block in the spinal monosynaptic pathway.

Asphyxiation of the spinal cord for periods of 2-4 min leads to block of the monosynaptic pathway. At about the same time this blockage takes place, the afferent action potentials fail to invade the presynaptic terminals. Asphyxiation also interferes with the antidromic invasion of motoneurons, and the failure of the antidromic action potentials to invade the motoneuron dendrites coincides with the time of the disappearance of the orthodromic monosynaptic responses. During reoxygenation, both the presynaptic terminals and the dendrites recover their function, or rather their polarization, in a few seconds and yet synaptic transmission reappears only after several minutes. It is postulated that failure of synaptic transmission during asphyxia is due to depolarization of both the presynaptic terminals and the dendrites of the postsynaptic elements. However, repolarization of these elements during reoxygenation, is not sufficient to reestablish synaptic transmission, but recovery of some unidentified biochemical process is apparently necessary.

Quantitative measures of the thermal reactivity of cutaneous mechanoreceptors.

Quantitative aspects of the non-specific response of cutaneous mechanoreceptors to two different modalities of stimulation were examined. Parameterization of stimulus temperature reveals the incompleteness of the commonly accepted criterion for thermal sensitivity and suggests the need for a re-examination of current concepts of specific mechanical, thermal and nociceptive sensibility.